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Clinical Oncology > Systemic Therapy > Flashcards

Systemic Therapy Flashcards

1
Q

What are some examples of alkylating agents. What is their mechanism of action

A

Cyclophosphamide
Dacarbazine
Nitroureas: lomustine, carmustine (cross blood brain barrier)
Temozolamide

Generally replace hydrogen in dna and other molecules with alkyl groups. Many have other cytotoxic actions

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2
Q

What is the mechanism of action of platinum compounds

A

Cisplatin, carboplatin, oxaliplatin
Cause inter strand and intra strand dna cross linking, preventing dna synthesis

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3
Q

What is the most common athracycline. What is the mechanism of action and main toxicity of concern

A

Adriamycin (doxorubicin)
Binds to dna, preventing dna and rna synthesis.
Cardiac toxicity is main concern (cardiomyopathy)
Myelosuppression is also a dose limiting toxicity

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4
Q

What are examples of antibiotics used in cancer treatment

A

Adriamycin/doxorubicin
Bleomycin
Mitomycin C (myelosuppression common)

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5
Q

What are examples of anti metabolite chemotherapy agents, and their mechanism of action

A

Methotrexate: folic acid antagonist. Prevents production of nucleotides
5-FU: structural analogue of thymine that irreversibly inhibits an enzyme important for thymine synthesis.
Hydroxyurea: inhibits an enzyme that in key in DNA synthesis.

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6
Q

What are examples of vinca alkaloids, and what is their mechanism of action

A

Vincristine, vinblastine.
Prevent microtubule formation, causing M-phase arrest

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7
Q

What is the mechanism of action of taxanes, and what are examples

A

Cause microtubule stabilisation, preventing cell progressing from mitosis phase
Paclitaxel: naturally occurring from Yew treee
Docetaxel: synthetic

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8
Q

What is a targeted monoclonal antibody against EGFR. Where does it act

A

Cetuximab
Acts on the extra cellular ligand receptor

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9
Q

What is a targeted therapy against VEGF

A

Bevacizumab

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10
Q

What are examples of BRAF V600E inhibitors

A

Vemurafenib
Dabrafenib

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11
Q

What type of targeted therapy is Imatinib. What are it’s targets and associated cancers it is used for

A

A tyrosine kinase inhibitor active against multiple tyrosine kinases

ABL (Philadelphia chromosome): CML, ALL
KIT: GIST, melanoma
PDGFRA

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12
Q

What is sunitinib and what cancers is it used for

A

Multi target tyrosine kinase inhibitor
-renal cancer
-GIST resistant to Imatinib

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13
Q

What are examples of first line and third line EGFR TKIs

A

1st: erlotinib, gefitinib
3rd line: osimertinib

Frequent to get acquired mutations on first gen tkis that render the tumour resistant. T790M most common

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14
Q

What is an example of an ALK inhibitor

A

Alectanib

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15
Q

What is the impact of MMRd on systemic treatment in colon cancer

A

Resistance to 5fu
More responsive to immune checkpoint inhibitors
More responsive to irinotecan

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16
Q

What is Denosumab, what is its use and mechanism of action

A

A RANK ligand inhibitor
Prevents maturation/ development of osteoclasts
Meta-analysis evidence they are better than bisphosphonates at reducing fracture related to Mets to bone

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17
Q

What is the mechanism of action of trastuzumab-emtansine

A

T-DM1
Drug conjugate that gets internalised into cells when binding to HER2 receptors. DM1 is then released which is cytotoxic and causes mitotic arrest

18
Q

What is the benefit of adjuvant zoledronate in the setting of breast cancer

A

Improves disease free survival

19
Q

What is the mechanism of action of palbociclib. What study supports its use

A

It is a selective CDK4/6 inhibitor.
Indicated for use in ER positive, HER-2 negative breast cancer
Paloma 2 trial showed significantly longer progression free survival. Longer data for OS benefit pending

20
Q

What is the function of fulvestrant

A

It’s is a selective estrogen receptor degrader (SERD)

21
Q

What are the treatment options for a well differentiated neuroendocrine tumour requiring treatment

A

Mainstay is surgical resection

Interventional radiology: ablation or embolisation

Systemic:
-octreotide (symptomatic control of functional tumours as well as anti proliferative effects)
-carbo/cis platin/etoposide: for rapidly progressive disease
-everolimus
-sunitinib

22
Q

What class of medications may be particularly useful for triple negative breast cancers

A

Immune checkpoint inhibitors. They typically express high levels of neoantigens

23
Q

For LCIS what is the relevance of pagetoid spread and Paget’s disease of the nipple

A

Pagetoid spread of cells is a feature; ie presence of individual discohesive cells between the basement membrane and luminal cells.
Paget’s disease of the nipple DOES NOT occur in LCIS. This is associated with DCIS +/- invasive carcinoma

24
Q

What is the mechanism of action of tamoxifen

A

Selective oestrogen receptor blockade

25
Q

What is the mechanism of action of anastrozole

A

Inhibits the aromatise enzyme, which prevents conversion of androgens into estrogens in peripheral tissues.
Post menopause this is a key source of oestrogen production, whereas in menstruating women the ovaries will still produce estrogen and aromatise inhibitors will therefore be ineffective

26
Q

What is the mechanism of action of PARP inhibitors, why are they only effective where BRCA mutations are present

A

Inhibit the protein PARP. PARP works alongside BRCA in HRR. When BRCA is mutated PARP still partially repairs DNA, leaving cells viable and capable to malignant growth. PARP inhibitors stop this repair so that the degree of DNA damage is overwhelming and the cells die.

They would not be effective in the absence of BRCA mutation as BRCA would repair the bulk of DNA dsbs

27
Q

What is the mechanism of action of abiraterone

A

It inhibits CYP17A1. This enzyme is part of pathways producing androgens, and therefore reduces the levels of androgens produced

28
Q

Why does prednisone need to be given with abiraterone

A

Alongside reducing the production of multiple androgens, it also inhibits glucocorticoid synthesis, resulting in glucocorticoid deficiency and mineralocorticoid excess.

29
Q

What agents are most established to have activity against soft tissue sarcomas

A

Doxorubicin
Ifosfamide

30
Q

What are frequent toxicities of ifosfamide

A

Neurotoxicity
Myelosuppression
Haemorrhagic cystitis

31
Q

What is the current evidence for systemic therapy in meningioma

A

Classical cytotoxics, octreotide, anti hormone therapy shows limited efficacy

There is a lack of phase 3 evidence, but potential role for several other agents:
-Pi3K and mTOR inhibitors (everolimus)
-immune checkpoint inhibitors
-CDK inhibitors
-TKIs
-bevacizumab

32
Q

Where do EGFR TKIs act

A

Enter the cell and act on the intracellular/cytoplasmic aspect of the receptor

33
Q

What EGFR muation is associated with the development of resistance to first line TKIs. What is the relevance prognostically

A

T790M
Accounts for 50% of erlotinib/gefitinib resistance
Less aggressive tumours than those that have TKI resistance due to other mechanisms

34
Q

What are first gen and second gen TKIs against ALK. What is the key benefit to the second gen

A

1st: crizotinib
2nd: alectanib. ALEX study demonstrated reduced cumulative incidence of CNS progression

35
Q

What TKI is used for ROS1 gene rearrangement

A

Crizotinib

36
Q

What is the name of the anti-CD38 antibody

A

Daratumumab

37
Q

What is the standard treatment regimen for multiple myeloma if the patient is fit for transplant

A

VCD: bortezomib, cyclophosphamide, lenalidomide

Followed by Melphalan then autologous stem cell transplant

38
Q

What is standard 1st line treatment for multiple myeloma if patient is unsuitable for transplant

A

Bortezomib, lenalidomide, dexamethasone

39
Q

What is imiquimod and what are it’s indications

A

A topical immune modulator

Indications:
-actinic keratosis
-BCC
-genital warts
Off label:
-lentigo maligna melanoma
-bowens disease (intraepidermal carcinoma/ SqCC in situ)

40
Q

What is the standard of care systemic therapy for unresectable HCC

A

Atezolizumab + bevacizumab

Clinical Oncology (2 decks)

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